Recent experimental evidence indicates that skeletal muscle blood flow is lower during pulsatile as compared to non-pulsatile perfusion. These pressure-flow studies have been primarily descriptive and have provided little insight as to the exact mechanism(s) by which pulsatility influences skeletal muscle vascular resistance. The most direct explanation of this response may be that the arterioles are sensitive to the rate of change to pressure as well as to the mean level somewhat as seen in the baroreceptors. However, redistribution of flow at the capillary level under the influence of pulsatile pressure could also account for the change in arteriolar tone by mechanisms more closely associated with tissue metabolism. Also, blood viscosity may be different under conditions of pulsatile flow. The proposed research is a microvascular approach, aimed at evaluating each of the mechanisms by which pulsatility may influence muscle vascular resistance. These proposed experiments will use the isolated, autoperfused cat sartorious muscle microvascular preparation in which changes in tissue oxygen tension, microvascular dimensions, pressures, and flows are quantified during experimental manipulations of pulse rate and amplitude. These studies should enable us to determine whether the arterioles are excited to contract by the pulsatile pressure or whether the increased vascular resistance is secondary to other changes as indicated above. The proposed study will also evaluate any pulse induced passive expansion of the arteriolar network against any active vasodilatory capabilities of the arteriolar pulse by examining changes in microvascular pressures, dimensions, and flows elicited by the arteriolar pulse in active versus passive preparations. The study is designed to critically evaluate the role of pulsatility in local blood flow regulation as well as to provide additional insight into the mechanisms of skeletal muscle blood flow control.